AMD is one of the causes of blindness, and is associated with degeneration to retinal photoreceptor cells of the macula corresponding to the center of the ocular fundus. AMD is primarily classified into an atrophic form (dry type) and exudative form (wet type). In the atrophic form, photoreceptor cells along with retinal pigment epithelial cells and choroidal capillaries adjacent thereto gradually undergo degenerative atrophy. In the exudative form, choroidal vascularization occurs resulting in comparatively rapid progression of the disease due to hemorrhage and edema. In human atrophic AMD, degeneration (thinning and reduction) of retinal pigment epithelium (RPE) and thinning and loss of the outer nuclear layer (ONL) are observed in the retina.
A light-induced retinopathy model is known as an animal model that mimics atrophic AMD (see, for example, Non-Patent Document 1). In this model, intense light is used to induce retinopathy. In actuality, degeneration of the retina has been confirmed to occur in a mouse model of light-induced retinopathy. In addition, there are some AMD-like animal models in rodents and rabbits in which RPE have been caused to degenerate by systemic or intravitreal administration of sodium iodate (see, for example, Non-Patent Document 2 or 3).
In general, in the development of drugs for treatment of a disease, animal models of the disease are needed to investigate the therapeutic effects of a test substance. In order to obtain a proper evaluation of pharmacological efficacy using an animal model, it is imperative that the animal model used accurately reflect the pathology of the target disease. Since non-human primates are genetically, neuroanatomically and pharmacokinetically closer to humans than rodents, they can be expected to allow the obtaining of actions and effects that more closely approximate the actions and effects observed during administration to humans. Consequently, in order to develop a therapeutic drug that is effective in humans, it is preferable to use non-human primates as an animal model instead of rodents. Since the macula in particular is only present in primates, animal models of AMD using rodents or rabbits do not reflect the pathology of human AMD. Therefore, in order to develop preventive and therapeutic drugs for AMD, a non-human primate model of AMD is required that more accurately reflects the pathology of AMD.